Balneotherapy in dermatology

Abstract

Balneotherapy and spa therapy emerged as an important treatment modality in the 1800s, first in Europe and then in the United States. Balneotherapy involves immersion of the patient in mineral water baths or pools. Today, water therapy is being practiced in many countries. Examples of unique and special places for balneotherapy are the Dead Sea in Israel, the Kangal hot spring in Turkey, and the Blue Lagoon in Iceland. Bathing in water with a high salt concentration is safe, effective, and pleasant for healing and recovery. This approach needs no chemicals or potentially harmful drugs. There are almost no side effects during and after treatment, and there is a very low risk to the patient's general health and well-being. Mineral waters and muds are commonly used for the treatment of various dermatologic conditions. The major dermatologic diseases that are frequently treated by balneotherapy with a high rate of success are psoriasis and atopic dermatitis. The mechanisms by which broad spectrums of diseases are alleviated by spa therapy have not been fully elucidated. They probably incorporate chemical, thermal, mechanical, and immunomodulatory effects. The major importance of balneotherapy and spa therapy both individually and as complements to other therapies lies in their potential effectiveness after standard medical treatments have failed to give comfort to these patients.

Hydrogen sulfide impairs keratinocyte cell growth and adhesion inhibiting mitogen-activated protein kinase signaling

“…Sulfurs are able to penetrate the skin, and a sulfur-rich balneotherapy is known to be effective in the treatment of psoriasis. 22 This is the reason why we used NaHS at concentrations that are higher than those of endogenously produced HS À , but comparable to those found in most natural sources of sulfurs. According to earlier studies, keratinocytes of hyperplastic epidermis express high levels of pERK with the classical nuclear localization, whereas keratinocytes of normal skin show low pERKs levels with a main cytoplasmic localization.…”

“…15 However, the effects promoted by exogenous H 2 S on keratinocytes and/or skin-derived blasts have been poorly investigated. The specific interest derives from the potential applications of the results, as sulfur is able to penetrate the skin and a sulfur-rich balneotherapy, known to be effective in the treatment of psoriasis, 22 might turn useful also in other T-cell-mediated autoimmune diseases of the skin.…”

Spinal cord transection inhibits HR reduction in anesthetized rats immersed in an artificial CO2-hot spring bath

“…Balneotherapy and spa therapy emerged as important European treatment modalities during the 1800s (Matz et al 2003) that are still practiced in many countries today. Carbon dioxide (CO 2 ) balneotherapy using hot springs containing free CO 2 at concentrations above 1 g·L -1 (ppm) (CO 2 -hot spring) has long been clinically applied to improve cardiovascular symptoms (Savin et al 1995;Toriyama et al 2002).…”

Hydrogen sulfide inhibits IL-8 expression in human keratinocytes via MAP kinase signaling

“…25 According to previous studies, keratinocytes of hyperplastic epidermis express high levels of pERK and IL-8. pERKs show the classical nuclear localization, while keratinocytes of normal skin show low pERKs levels with a main cytoplasmic localization.…”

“…21,22 Many studies have been published on the involvement of hydrogen sulfide in inflammation, and evidence has been shown for both pro-or anti-inflammatory roles of H 2 S. 23,24 Recently, we have demonstrated that hydrogen sulfide can impair human keratinocytes adhesion and proliferation by impairing the activation of Raf-MEK-ERK pathway. 22 The specific interest to hydrogen sulfide derives from the potential applications of the results, as sulfur is able to penetrate the skin and a sulfur-rich balneotherapy, known to be effective in the treatment of psoriasis, 25 might turn useful in this disease. In this context, we have also demonstrated that H 2 S can exert a subset-specific toxicity on peripheral blood lymphocytes, which die by a caspase-independent mechanism of necrosis after a rapid loss of mitochondrial membrane potential, and not by apoptosis.…”